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Expression of a bovine growth hormone transgene inhibits pregnant mare's serum gonadotropin-induced follicle maturation in prepuberal gilts

Guthrie, H.D., Pursel, V.G., Bolt, D.J., Cooper, B.S.
Journal of animal science 1993 v.71 no.12 pp. 3409
gilts, somatotropin, pregnant mare serum gonadotropin, follicular fluid, gene expression, androstenedione, progesterone, inhibin, transgenic animals, ovarian follicles
Prepuberal gilts were injected with PMSG to determine whether expression of a bovine growth hormone (bGH) transgene inhibited preovulatory maturation of ovarian follicles. Seven transgenic (TG) gilts of line 3706, which expresses a mouse metallothionein-bGH transgene, and eight nontransgenic, control (C) gilts (128 to 147 d old) were injected with PMSG, 12.5 IU/kg BW, 72 h before necropsy. Surface ovarian follicles > 1 mm in diameter were counted, measured for diameter, and aspirated for fluid. Follicles were classified morphologically as healthy or atretic and those with follicular fluid estradiol-17 beta > 100 ng/mL were classified as estrogen-active (EA). The number of follicles per gilt was 64.3 +/- 6.1 (mean +/- SEM) and did not differ significantly between bGH-TG and C gilts. The PMSG treatment induced growth of large (> 5 mm) follicles in both bGH-TG and C gilts. However, compared with C gilts, bGH-TG gilts had fewer (P <.05) large follicles (5.9 +/- 1.5 vs 18.3 5.4), a lower proportion of EA large follicles (35 +/- 12.5 vs 69 +/- 13.2%), and in large follicles less (P < .05) estradiol-17 beta (86 +/- 17 vs 350 +/- 69 ng/mL) and androstenedione (300 +/- 33 vs 1,283 +/- 221 ng/mL). Follicular fluid progesterone and inhibin did not differ significantly between bGH-TG and C gilts. The incidence of atresia among small and medium follicles did not differ significantly between bGH-TG and C gilts. These results indicate that chronic, unregulated expression of a bGH transgene in prepuberal gilts inhibited follicle growth in response to administration of PMSG and may have blocked estradiol-17 beta production in vivo by inhibiting theca interna androgen production.